The hypothesis proposed in this review provides a novel view of both the control of feeding and the function of brown adipose tissue (BAT) thermogenesis. It takes into account the episodic nature of feeding in rats allowed free access to food and the necessity for episodic events in the controlling systems which govern initiation and termination of feeding. A feeding episode is proposed to occur during an episode of increased sympathetic nervous system activity that stimulates BAT thermogenesis and increases body temperature. Two different aspects of stimulated BAT metabolism, namely increased uptake of glucose and increased heat production, evoke initiation and termination of feeding, respectively. Initiation is mediated by a transient dip in blood glucose concentration caused by stimulated glucose utilization in BAT. Feeding continues while both BAT and core temperature continue to rise. Termination is induced by the high level of core temperature brought about by the episode of stimulated BAT thermogenesis. The time between initiation and termination determines the size of the meal and depends on the balance between BAT thermogenesis and heat loss, and thus on ambient temperature. The underlying cause of the episodic stimulation of sympathetic nervous system activity is a decline in core temperature to a level recognized by the hypothalamus as needing a burst of increased heat production. Thus, BAT thermogenesis is important in control of meal size, relating it to thermoregulatory needs. When this function is lost, as in many obese animal models of obesity, the animal loses its ability to remain in energy balance by precisely adjusting its intake in relation to environmental temperature and meal size increases. The hypothesis also predicts that an increase in endogenous heat production that is not due to BAT thermogenesis will prevent the matching of intake to increased expenditure via thermoregulatory feeding.